5,6-Dichlorobenzimidazole riboside
Based on 9 publication(s) in Google Scholar
5,6-Dichlorobenzimidazole riboside (DRB) is a nucleoside analog that inhibits several carboxyl-terminal domain kinases, including casein kinase II and cell cycle-dependent kinases (CDK). 5, 6-dichlorobenzimidazole riboside has antitumor activity. 5, 6-dichlorobenzimidazole riboside can induce apoptosis.
For research use only. We do not sell to patients.
- Purity : 99.89%
- CAS No.: 53-85-0
- Formula: C12H12Cl2N2O4
- Molecular Weight:319.14
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Storage:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
Publications Citing Use of MedChemExpress (MCE) 5,6-Dichlorobenzimidazole riboside
More- J Extracell Vesicles. 2024 Aug;13(8):e12488. [Abstract]
- Mol Cell. 2025 Sep 18;85(18):3425-3442.e10. [Abstract]
- Mol Cell. 2025 Apr 3;85(7):1280-1295.e9. [Abstract]
- Cell Rep. 2022 Oct 25;41(4):111546. [Abstract]
- bioRxiv. 2025 Oct 11.
- bioRxiv. 2025 Aug 19.
- bioRxiv. 2025 May 24.
- bioRxiv. 2025 April 14.
- bioRxiv. 2024 July 27.
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RT-PCR
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RT-PCR
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| BSC-1 | IC50 |
30 μM
Compound: 1f
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Antiviral activity against HSV-1 (herpes simplex virus), determined by ELISA in quadruplicate wells using BSC-1 cells
Antiviral activity against HSV-1 (herpes simplex virus), determined by ELISA in quadruplicate wells using BSC-1 cells
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[PMID: 10882370] |
| carcinoma cell line | IC50 |
36 μM
Compound: DRB
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Compound was tested for inhibition activity of human oral carcinoma cell line (KB ) cells in quadruplicate assay.
Compound was tested for inhibition activity of human oral carcinoma cell line (KB ) cells in quadruplicate assay.
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[PMID: 10882375] |
| HCT-116 | GI50 |
25 μM
Compound: DRB
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Cytotoxicity against human HCT116 cells after 48 hrs by MTT assay
Cytotoxicity against human HCT116 cells after 48 hrs by MTT assay
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[PMID: 22225635] |
| HFF | IC50 |
24 μM
Compound: DRB
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Cytotoxicity produced in human foreskin fibroblasts (HFF) cells was estimated by visual scoring of cells unaffected by virus infection in the plaque-reduction assay.
Cytotoxicity produced in human foreskin fibroblasts (HFF) cells was estimated by visual scoring of cells unaffected by virus infection in the plaque-reduction assay.
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[PMID: 8784445] |
| HFF | IC50 |
24 μM
Compound: 1f
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Visual cytotoxicity against stationary human foreskin fibroblasts (HFF) cells at the time of HCMV plaque enumeration
Visual cytotoxicity against stationary human foreskin fibroblasts (HFF) cells at the time of HCMV plaque enumeration
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[PMID: 10882370] |
| HFF | IC50 |
24 μM
Compound: DRB
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Compound was tested for visual cytotoxicity on human foreskin fibroblasts (HFF) cells
Compound was tested for visual cytotoxicity on human foreskin fibroblasts (HFF) cells
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[PMID: 10882375] |
| HFF | IC50 |
24 μM
Compound: DRB
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Compound was evaluated for the visual cytotoxicity scored on HFF cells at time of HCMV plaque enumeration
Compound was evaluated for the visual cytotoxicity scored on HFF cells at time of HCMV plaque enumeration
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[PMID: 7562945] |
| HFF | IC50 |
24 μM
Compound: DRB
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Tested for the visual cytotoxicity on HFF cells at the time of human cytomegalovirus (HCMV) plaque enumeration
Tested for the visual cytotoxicity on HFF cells at the time of human cytomegalovirus (HCMV) plaque enumeration
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[PMID: 8071942] |
| HFF | IC50 |
24 μM
Compound: DRB
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Cytotoxicity against human foreskin fibroblasts (HFF) cells
Cytotoxicity against human foreskin fibroblasts (HFF) cells
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10.1016/S0960-894X(00)80628-9 |
| HFF | IC50 |
42 μM
Compound: 1f
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Antiviral activity against towne strain HCMV was determined by plaque reduction assay in duplicate wells using HFF cells
Antiviral activity against towne strain HCMV was determined by plaque reduction assay in duplicate wells using HFF cells
|
[PMID: 10882370] |
| HFF | IC50 |
42 μM
Compound: DRB
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Compound was tested for antiviral activity against human cytomegalovirus (HCMV) by plaque reduction assay using HFF cells
Compound was tested for antiviral activity against human cytomegalovirus (HCMV) by plaque reduction assay using HFF cells
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[PMID: 10882375] |
| Huh-7 | CC50 |
40.4 μM
Compound: DRB
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Cytotoxicity against dual-reporter HCV replicon Huh7 cells by measuring XTT end points after 72 hrs
Cytotoxicity against dual-reporter HCV replicon Huh7 cells by measuring XTT end points after 72 hrs
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[PMID: 17060518] |
| Huh-7 | CC50 |
60.7 μM
Compound: DRB
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Cytotoxicity against dual-reporter HCV replicon Huh7 cells by measuring FLuc reporter activity after 72 hrs
Cytotoxicity against dual-reporter HCV replicon Huh7 cells by measuring FLuc reporter activity after 72 hrs
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[PMID: 17060518] |
| Huh-7 | EC50 |
34.1 μM
Compound: DRB
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Antiviral activity against HCV 1b con1 in dual-reporter HCV replicon Huh7 cells by measuring hRLuc reporter activity after 72 hrs
Antiviral activity against HCV 1b con1 in dual-reporter HCV replicon Huh7 cells by measuring hRLuc reporter activity after 72 hrs
|
[PMID: 17060518] |
| KB | IC50 |
100 μM
Compound: DRB
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The inhibition of KB cell growth was determined
The inhibition of KB cell growth was determined
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[PMID: 8071942] |
| KB | IC50 |
36 μM
Compound: 1f
|
Compound was tested for the inhibition of KB cell growth in quadruplicate wells
Compound was tested for the inhibition of KB cell growth in quadruplicate wells
|
[PMID: 10882370] |
| KB | IC50 |
36 μM
Compound: DRB
|
Compound was evaluated for the inhibition of KB cell growth determined in quadruplicate assay
Compound was evaluated for the inhibition of KB cell growth determined in quadruplicate assay
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[PMID: 7562945] |
| KB | IC50 |
36 μM
Compound: DRB
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Inhibitory activity against growth of human epidermoid oral carcinoma KB cell line
Inhibitory activity against growth of human epidermoid oral carcinoma KB cell line
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[PMID: 8784445] |
| LP-1 | IC50 |
29.81 μM
Compound: DRB
|
Cytotoxicity against human LP-1 cells after 72 hrs by alamar blue assay
Cytotoxicity against human LP-1 cells after 72 hrs by alamar blue assay
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[PMID: 15958589] |
| MCF7 | GI50 |
36 μM
Compound: DRB
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Cytotoxicity against human MCF7 cells after 48 hrs by MTT assay
Cytotoxicity against human MCF7 cells after 48 hrs by MTT assay
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[PMID: 22225635] |
| NCI-H929 | IC50 |
20.13 μM
Compound: DRB
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Cytotoxicity against human NCI-H929 cells after 72 hrs by alamar blue assay
Cytotoxicity against human NCI-H929 cells after 72 hrs by alamar blue assay
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[PMID: 15958589] |
| OPM-2 | IC50 |
29.52 μM
Compound: DRB
|
Cytotoxicity against human OPM2 cells after 72 hrs by alamar blue assay
Cytotoxicity against human OPM2 cells after 72 hrs by alamar blue assay
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[PMID: 15958589] |
| RPMI-8226 | IC50 |
46.79 μM
Compound: DRB
|
Cytotoxicity against human RPM18226 cells after 72 hrs by alamar blue assay
Cytotoxicity against human RPM18226 cells after 72 hrs by alamar blue assay
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[PMID: 15958589] |
| U-266 | IC50 |
41.02 μM
Compound: DRB
|
Cytotoxicity against human U266 cells after 72 hrs by alamar blue assay
Cytotoxicity against human U266 cells after 72 hrs by alamar blue assay
|
[PMID: 15958589] |
In Vitro
5,6-Dichlorobenzimidazole riboside (10-80 μg/mL, 72 h) induces p53-dependent apoptosis of human colon cancer cells by blocking RNA synthesis[5].
5,6-Dichlorobenzimidazole riboside (10-100 μM, 72 h) induces apoptosis of human MCF-7 breast cancer cells by regulating Mcl-1 and BclxL. And activates members of the caspase family in a time - and dose-dependent manner[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:LS174T, HT29, SW48
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Concentration:80 μg/mL
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Incubation Time:24 h
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Result:Decreased incorporation of [5,6-3H] uridine and increased level of p53 protein.
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Cell Line:MCF-7, T-47D
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Concentration:10, 50, 75,100 μM
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Incubation Time:72 h
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Result:Inhibited cell-growth in a dose-dependent manner. Resulted in a higher early apoptotic population (5.7 ± 1.1 vs. 2 ± 0.4%) and late apoptotic population (15.9 ± 2.4 vs. 7.7 ± 0.9%) at a concentration of 75 μM.
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Cell Line:MCF-7
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Concentration:75 μM
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Incubation Time:0.5, 2, 6, 10 h
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Result:Reduced Mcl-1 protein levels in a time-dependent manner and increased the level of p53 after 6 h.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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CAS No. 53-85-0
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Appearance Solid
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Molecular Weight 319.14
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Formula C12H12Cl2N2O4
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Color White to off-white
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SMILES
OC[C@@H]1[C@@H](O)[C@@H](O)[C@H](N2C3=CC(Cl)=C(Cl)C=C3N=C2)O1
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Synonyms
DRB
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Publications (9)
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Journal Impact Factor
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Most Recent
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J Extracell Vesicles
Extracellular vesicles miR-31-5p promotes pancreatic cancer chemoresistance via regulating LATS2-Hippo pathway and promoting SPARC secretion from pancreatic stellate cells. [Abstract]2024 Aug;13(8):e12488. PMID: 39104296
5,6-Dichlorobenzimidazole riboside purchased from MedChemExpress. Usage Cited in: J Extracell Vesicles. 2024 Aug;13(8):e12488. [Abstract]
PANC-1 EVs upregulated miR-31-5p levels in PSCs even under DRB (5,6-Dichlorobenzimidazole riboside, 10 μM) treatment.
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Mol Cell
2025 Sep 18;85(18):3425-3442.e10. PMID: 40914169 -
Mol Cell
Transcription-coupled AID deamination damage depends on ELOF1-associated RNA polymerase II. [Abstract]2025 Apr 3;85(7):1280-1295.e9. PMID: 40049162 -
Cell Rep
m6A modification confers thermal vulnerability to HPV E7 oncotranscripts via reverse regulation of its reader protein IGF2BP1 upon heat stress. [Abstract]2022 Oct 25;41(4):111546. PMID: 36288717
5,6-Dichlorobenzimidazole riboside purchased from MedChemExpress. Usage Cited in: Cell Rep. 2022 Oct 25;41(4):111546. [Abstract]
Transcription inhibitors does not affect heat-mediated E7 mRNA downregulation. CaSki (E) and SiHa (F) cells were pretreated with or without two transcription inhibitors, triptolide and DRB (5,6-Dichlorobenzimidazole riboside) for 60 min, and subjected to HT (42℃, 60 min). Relative expression levels of E7, HSP70 and β-Actin mRNAs were measured by RT-qPCR.
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Solvent & Solubility
In Vitro:
DMF : 100 mg/mL (313.34 mM; Need ultrasonic)
DMSO : 100 mg/mL (313.34 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Ethanol : 7.69 mg/mL (24.10 mM; Need ultrasonic)
H2O : < 0.1 mg/mL (insoluble)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.5 mg/mL (7.83 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (7.83 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocols
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Flow cytometric DNA-content cell-cycle staining
Flow cytometric DNA-content cell-cycle staining measures the fluorescence intensity of DNA-bound fluorochromes in single cells or nuclei to estimate DNA content distributions, allowing assignment of populations to G0/G1, S, and G2/M phases by DNA histogram deconvolution. Propidium iodide (PI) intercalates into DNA, and PI fluorescence is proportional to cellular DNA content when staining is performed under conditions that make DNA accessible and minimize non-DNA signal. Cells with G2/M DNA content are expected to show approximately twice the fluorescence intensity of G0/G1 cells, while S-phase cells occupy intermediate fluorescence values. PI-based DNA-content analysis can also detect cells with fractional DNA content, often reported as sub-G1, when DNA fragmentation and extraction during staining reduce retained DNA signal in apoptotic cells. DAPI is an alternative DNA fluorochrome for univariate DNA-content analysis, while bivariate approaches combining DNA content with proliferation
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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BrdU Incorporation Assay
Bromodeoxyuridine (BrdU) incorporation assay is based on the principle that BrdU, a thymidine analog, is incorporated into newly synthesized DNA during the S phase of the cell cycle, thereby serving as a marker of DNA replication and cellular proliferation. Incorporated BrdU can be detected using anti-BrdU antibodies following DNA denaturation, enabling visualization or quantification of proliferating cells through immunochemical detection methods such as immunofluorescence or immunohistochemistry.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Protocol for Cell Cycle
Cell-cycle analysis by flow cytometry measures DNA content in single cells to estimate the fraction of cells in G0/G1, S, and G2/M phases. Propidium iodide intercalates into DNA, and after RNA removal with RNase, fluorescence intensity reflects cellular DNA content: 2N cells are assigned to G0/G1, cells between 2N and 4N to S phase, and 4N cells to G2/M. DNA-content analysis alone cannot reliably separate G0 from G1 or G2 from M. Ki-67 can distinguish quiescent G0 cells from cycling cells, EdU or BrdU incorporation marks active DNA synthesis in S phase, and phospho-histone H3 staining identifies mitotic cells within the 4N population.
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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
Purity & Documentation
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Data Sheet (283 KB)
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SDS (396 KB)
- English - EN (396 KB)
- Français - FR (396 KB)
- Deutsch - DE (396 KB)
- Norwegian - NO (396 KB)
- Español - ES (396 KB)
- Swedish - SV (396 KB)
- Italian - IT (396 KB)
- Korean - KR (396 KB)
- Portuguese - PT (396 KB)
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Handling Instructions (2659 KB)
References
[1]. Zandomeni RO. Kinetics of inhibition by 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole on calf thymus casein kinase II. Biochem J. 1989 Sep 1;262(2):469-73. [Content Brief]
[2]. Yankulov K, et al. The transcriptional elongation inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole inhibits transcription factor IIH-associated protein kinase. J Biol Chem. 1995 Oct 13;270(41):23922-5. [Content Brief]
[3]. Rickert P, et al. Cyclin C/CDK8 and cyclin H/CDK7/p36 are biochemically distinct CTD kinases. Oncogene. 1999 Jan 28;18(4):1093-102. [Content Brief]
[4]. Schang LM. Cyclin-dependent kinases as cellular targets for antiviral drugs. J Antimicrob Chemother. 2002 Dec;50(6):779-92. [Content Brief]
[5]. te Poele RH, et al. RNA synthesis block by 5, 6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) triggers p53-dependent apoptosis in human colon carcinoma cells. Oncogene. 1999 Oct 14;18(42):5765-72. [Content Brief]
[6]. Kuo YH,et al. 5,6-Dichloro-1-β-D-ribofuranosylbenzimidazole (DRB) induces apoptosis in breast cancer cells through inhibiting of Mcl-1 expression. Sci Rep. 2023 Aug 3;13(1):12621 [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| Ethanol / DMF / DMSO | 1 mM | 3.1334 mL | 15.6671 mL | 31.3342 mL | 78.3355 mL |
| 5 mM | 0.6267 mL | 3.1334 mL | 6.2668 mL | 15.6671 mL | |
| 10 mM | 0.3133 mL | 1.5667 mL | 3.1334 mL | 7.8336 mL | |
| 15 mM | 0.2089 mL | 1.0445 mL | 2.0889 mL | 5.2224 mL | |
| 20 mM | 0.1567 mL | 0.7834 mL | 1.5667 mL | 3.9168 mL | |
| DMF / DMSO | 25 mM | 0.1253 mL | 0.6267 mL | 1.2534 mL | 3.1334 mL |
| 30 mM | 0.1044 mL | 0.5222 mL | 1.0445 mL | 2.6112 mL | |
| 40 mM | 0.0783 mL | 0.3917 mL | 0.7834 mL | 1.9584 mL | |
| 50 mM | 0.0627 mL | 0.3133 mL | 0.6267 mL | 1.5667 mL | |
| 60 mM | 0.0522 mL | 0.2611 mL | 0.5222 mL | 1.3056 mL | |
| 80 mM | 0.0392 mL | 0.1958 mL | 0.3917 mL | 0.9792 mL | |
| 100 mM | 0.0313 mL | 0.1567 mL | 0.3133 mL | 0.7834 mL |